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Year : 2022  |  Volume : 6  |  Issue : 2  |  Page : 155

Cutaneous arteriovenous malformation: successful treatment with embolization and excision – A case report

1 Department of Dermatology, Jawaharlal Institute of Postgraduate Medical Education and Research, Puducherry, India
2 Department of Dermatology, Pondicherry Institute of Medical Sciences, Puducherry, India
3 Department of Intervention Radiology, PSG Hospitals, Coimbatore, Tamil Nadu, India

Date of Submission01-Oct-2021
Date of Decision15-Feb-2022
Date of Acceptance04-Jun-2022
Date of Web Publication26-Aug-2022

Correspondence Address:
Remya Raj Rajamohanan
Department of Dermatology, Pondicherry Institute of Medical Sciences, Puducherry - 605 014
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/cdr.cdr_89_21

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How to cite this article:
Sakkaravarthi V, Rajamohanan RR, Swamiappan E, Chandrashekar L. Cutaneous arteriovenous malformation: successful treatment with embolization and excision – A case report. Clin Dermatol Rev 2022;6:155

How to cite this URL:
Sakkaravarthi V, Rajamohanan RR, Swamiappan E, Chandrashekar L. Cutaneous arteriovenous malformation: successful treatment with embolization and excision – A case report. Clin Dermatol Rev [serial online] 2022 [cited 2023 Feb 3];6:155. Available from: https://www.cdriadvlkn.org/text.asp?2022/6/2/155/354763


A 25-year-old male came to our outpatient department with complaints of a slowly growing nodule over his left chest wall for 6 months. The patient gave a history of pain, spontaneous ulceration, and bleeding from the nodule for the past 2 months. He had encountered a blunt trauma over the same site 2 years ago without any external injuries. He had no systemic ailments. Physical examination revealed a single erythematous exophytic nodule of size 4 cm × 4 cm located on the left lateral thoracic wall. The surface of the nodule revealed multiple bluish nodules and hemorrhagic crusts [Figure 1]a. The nodule was firm, warm, and nontender with thrill and bruit. It was noncompressible, and its size did not vary on assuming the dependent position. There was no evidence of volume overload in him. Physical examination ruled out cranial or spinal involvement. There were no episodes of spontaneous nasal bleeds in the past and no family history of tumors or vascular malformation.
Figure 1: (a) Nodule over the left lateral thoracic wall with surface showing bluish nodules and hemorrhagic crusting (b) same site following embolization and excision of the nodule

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Routine laboratory investigations were normal. Magnetic resonance imaging (MRI) of the thorax revealed a radiodense mass at the level of the 7th intercostal plane extending up to the muscular plane without involving ribs and viscera [Figure 2]. Magnetic resonance angiography (MRA) confirmed that it was a high-flow vascular malformation of size 2.9 cm × 3.1 cm with feeding arteries from the left T6 and T7 anterior intercostal arteries and draining into the left axillary vein [Figure 3]. Both eye fundus examinations were normal. We performed MRI spine to rule out spinal arteriovenous malformation/arteriovenous (AVM/AV) fistula which was normal. MRI of the chest, abdomen, and pelvis was done to rule out visceral AVM.
Figure 2: Magnetic resonance imaging of the chest showing radiodense mass extending up to muscular plane without involvement of ribs and viscera

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Figure 3: Magnetic resonance angiography showing feeding arteries – left 6th and 7th anterior intercostal arteries

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Under local anesthesia, with the guide of digital subtraction angiography (DSA) using transfemoral catheterization of the internal thoracic artery, embolization of the tumor was done with 70% n-butyl cyanoacrylate–Lipoidal mixture using 18G lumbar puncture needle. Immediately after the embolization, the nodule was warm and hard without any pulsation or bruit. Postprocedure DSA showed 95% embolization of the nidus compared to the preprocedure DSA [Figure 4]a and [Figure 4]b. Three days after embolization, the tumor was completely excised with ligation of the feeder vessels [Figure 1]b. There was no recurrence up to 1 year following the procedure, after which the patient was lost to follow up.
Figure 4: (a) Preprocedure DSA showing both feeder arteries and nidus (b) Postprocedure DSA showing 95% embolization of the nidus. DSA: Digital subtraction angiography

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AVMs are a rare vascular anomaly that most commonly occurs in the brain. Extracranial or peripheral AVMs are extremely rare and most commonly have congenital etiology.[1] Intercostal AVMs are predominantly acquired secondary to trauma, infection, or iatrogenic procedures.[2],[3],[4] Congenital etiology was considered in our patient given the absence of penetrating injury to the intercostal region. The blunt trauma experienced by our patient might be the trigger for his congenital AVM to become apparent in adulthood. The various syndromes associated with AVM such as hereditary hemorrhagic telangiectasia, capillary malformation–AVM, Cobb syndrome, Parkes Weber syndrome, and Cowden syndrome were also ruled out in our patient.[5]

Complications arising from intercostal AVMs include disfigurement, bleeding, hemothorax, pneumothorax, bone erosion, pain, and congestive cardiac failure.[3] The clinical examination will often suggest the diagnosis of AVM. However, imaging is necessary to confirm the clinical diagnosis and to identify the extent of the lesion. Hand-held Doppler ultrasound is generally the initial imaging study of choice as it provides an early, safe, and inexpensive diagnosis of AVM by demonstrating the characteristic high-velocity flow of the lesion.[1],[6] MRI helps in the assessment of the extent of the lesion and its infiltration into the surrounding soft tissue. The role of MRA is in the evaluation of acute symptoms such as bleeding, to distinguish between high-flow and low-flow malformations, and also the preferred imaging modality posttreatment.[1]

For therapeutic purpose, AVMs are clinically staged using the Schobinger classification. Stage 1 lesions are asymptomatic, stage 2 are symptomatic with thrill and bruit, stage 3 includes lesions with complications such as bleeding, ulceration, pain, and necrosis, and stage 4 denotes the development of high-output cardiac failure. In general, stage 3 lesions and above should receive treatment, but the indication for treatment of lower stages remains controversial.[7] The therapeutic goal in AVM should be selective removal of the anomalous vessels while preserving the surrounding normal tissue. To accomplish this, a multidisciplinary team with expertise in various treatment modalities is required.[4] The choice of treatment will differ depending on the site, size, and stage of peripheral AVM. Treatment options include lasers, endovascular embolization, interstitial or intravascular sclerotherapy, en bloc resection of the vascular malformation, pharmacotherapy, or a combination of all these.[4] Endovascular embolotherapy can be done using liquid embolic agents such as ethanol, ethylene–vinyl alcohol copolymer (EVOH), Onyx and glue (n-butyl-cyanoacrylate [NBCA]) or microspheres, or mechanical occlusive devices such as plugs and coils.[8] However, for preoperative embolization, NBCA is preferred as it provides a focus to resect.[1] Liu et al.,[4] reported that resection offers long-term control for the localized AVM. The recurrence rate after embolization alone was higher (98%) compared to resection with or without embolization (81%).[4]

We would like to emphasize the role of dermatologists in the early recognition of this condition as we are often the primary point of contact for patients with peripheral AVMs with visible skin lesions. As a dermatologist, we must not perform invasive procedures such as biopsy or sclerotherapy in these vascular anomalies. A multidisciplinary team equipped to manage acute and life-threatening complications is required for the management of AVM.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient (s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Timbang MR, Richter GT. Update on extracranial arteriovenous malformations: A staged multidisciplinary approach. Semin Pediatr Surg 2020;29:150965.  Back to cited text no. 1
de Miguel R, López-Gutierrez JC, Boixeda P. Arteriovenous malformations: A diagnostic and therapeutic challenge. Actas Dermosifiliogr 2014;105:347-58.  Back to cited text no. 2
Parashi HS, Bhosle KN, Thakare ND, Sharma A, Potwar SS. Giant congenital intercostal arteriovenous malformation with extensive involvement of chest wall and ribs: Surgical experience. Ann Thorac Surg 2013;95:2157-9.  Back to cited text no. 3
Liu AS, Mulliken JB, Zurakowski D, Fishman SJ, Greene AK. Extracranial arteriovenous malformations: Natural progression and recurrence after treatment. Plast Reconstr Surg 2010;125:1185-94.  Back to cited text no. 4
Nozaki T, Nosaka S, Miyazaki O, Makidono A, Yamamoto A, Niwa T, et al. Syndromes associated with vascular tumors and malformations: A pictorial review. Radiographics 2013;33:175-95.  Back to cited text no. 5
Meredith O, Tollefson M. Use of handheld Doppler ultrasound in capillary malformation-arteriovenous malformation syndrome: A case report. J Am Acad Dermatol 2015;72.  Back to cited text no. 6
Lam K, Pillai A, Reddick M. Peripheral arteriovenous malformations: Classification and endovascular treatment. Appl Radiol 2017;46:15-21.  Back to cited text no. 7
Rivera PP, Kole MK, Pelz DM, Gulka IB, McKenzie FN, Lownie SP. Congenital intercostal arteriovenous malformation. AJR Am J Roentgenol 2006;187:W503-6.  Back to cited text no. 8


  [Figure 1], [Figure 2], [Figure 3], [Figure 4]


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